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C3 and C4 complement levels in AQP4-IgG-positive NMOSD and in MOGAD.

Authors :
Pache, Florence
Ringelstein, Marius
Aktas, Orhan
Kleiter, Ingo
Jarius, Sven
Siebert, Nadja
Bellmann-Strobl, Judith
Paul, Friedemann
Ruprecht, Klemens
Source :
Journal of Neuroimmunology. Nov2021, Vol. 360, pN.PAG-N.PAG. 1p.
Publication Year :
2021

Abstract

While complement-dependent cytotoxicity (CDC) is a known effector mechanism in aquaporin-4-immunoglobulin (Ig)G-positive (AQP4-IgG+) neuromyelitis optica spectrum disorder (NMOSD), the role of CDC in myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) is less clear. We determined complement C3 and C4 plasma concentrations in patients with clinically stable AQP4-IgG+ NMOSD (n = 16), MOGAD (n = 15), early multiple sclerosis (MS, n = 19) and in healthy controls (HC, n = 18). C4 was lower in AQP4-IgG+ NMOSD than in MOGAD, MS and HC (p < 0.05, pairwise comparisons). C3 was lower in AQP4-IgG+ NMOSD than in MS (p = 0.034). These findings suggest subtle complement consumption in clinically stable AQP4-IgG+ NMOSD, but not in MOGAD. [Display omitted] • Complement-dependent cytotoxicity (CDC) is a known effector mechanism in AQP4-IgG+NMOSD. • The role of CDC in myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) is less clear. • We measured complement C3 and C4 in plasma of patients with AQP4-IgG+ NMOSD, MOGAD, MS and healthy controls (HC). • C4 was lower in AQP4-IgG+ NMOSD than in MOGAD, MS and healthy controls. • These findings are compatible with a more prominent role of complement in AQP4-IgG+ NMOSD than in MOGAD. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
01655728
Volume :
360
Database :
Academic Search Index
Journal :
Journal of Neuroimmunology
Publication Type :
Academic Journal
Accession number :
152896076
Full Text :
https://doi.org/10.1016/j.jneuroim.2021.577699